Angiotensin II suppresses the insulin sensitivity via enhancement of serine phosphorylation of insulin receptor and suppression of tyrosine phosphorylation of IRS-1. Adiponectin increases insulin sensitivity, and TNF-alpha decreases insulin sensitivity. From our studies, the suppressed adiponectin and increased TNF-alpha may play an important role of the insulin resistance mechanisms. Angiotensin II suppresses the differentiation of adipocyte. Large sized adipocytes increase TNF-alpha and decrease adiponectin. Angiotensin II also has the direct stimulating action on TNF-alpha synthesis. ARB increases adiponectin a nddecreases TNF-alpha. Improvements of these adipocytokines dysfunction by ARB may concern tothe improvement of insulin resistance. The significance of various adipocytokines in insulin resistance and metabolic syndrome is also introduced.